SGU Episode 823

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SGU Episode 823
April 17th 2021
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SGU 822                      SGU 824

Skeptical Rogues
S: Steven Novella

B: Bob Novella

C: Cara Santa Maria

J: Jay Novella

E: Evan Bernstein

Guest

G: George Hrab

Quote of the Week

Common sense is a very tricky instrument. It is as deceptive as it is indispensable.

Susanne Katherina Langer

Links
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Show Notes
Forum Discussion


Introduction[edit]

Voice-over: You're listening to the Skeptics' Guide to the Universe, your escape to reality.

S: Hello and welcome to the Skeptics' Guide to the Universe. Today is Wednesday, April 14th. 2021, and this is your host, Steven Novella. Joining me this week are Bob Novella...

B: Hey, everybody!

S: Cara Santa Maria...

C: Howdy.

S: Jay Novella...

J: Hey guys...

S: ...and Evan Bernstein.

E: Hello everyone.

S: This was one of those heavy news weeks, heavy science news weeks. I suspect that two of the news items we're going to talk about this week are going to be two of the biggest science news items of the year. If not one and two, I think they'll both be in the top five. They're big. We'll get to them in a minute.

COVID-19 Update (0:45)[edit]

S: But first, there's another sort of big item that's a follow-up to last week. Last week I gave the follow-up to the AstraZeneca blood clot issue. This is the main European vaccine, AstraZeneca, for COVID, and there has been some reported blood clots. Most of them are probably not above background. However, there was one subset of clots in young people, like less than 50, mostly women, specifically in the brain, CVST, cerebral venous sinus thrombosis, associated with thrombocytopenia, low blood platelets, which are the clotting elements in the blood. So that was unusual.

B: Steve, isn't another factor that the symptoms arose within two to four weeks after the shot?

S: Yeah, within like 16 days or something. So they were within the time frame of the vaccine.

B: How could you have clotting and low platelet count? So I'm sure that's in your description somewhere.

S: Well, yeah, because their dysfunctional platelets is the problem, right? So there's low number, but they're causing clotting.

B: All right.

S: Yeah, and then there's been a couple of different publications, including one recently in the New England Journal of Medicine, looking at potential mechanisms. It's certainly plausible that it is a vaccine-induced autoimmune disease causing this clotting situation. But the numbers are extremely low, the absolute numbers, and there's still some heated debate about the risk versus benefit. You're going to be saving thousands of lives with the vaccine, and one or two people will die, that sort of thing. But we're comparing that to, but we don't want to freak people out about the vaccine, and we want to make sure we're being transparent, and yeah, so it's like this total mess. Well, the mess just got doubled because the Johnson & Johnson vaccine has the same thing now. There have been six reported cases of CVST, cerebral venous venous thrombosis, with thrombocytopenia in women between the ages of 18 and 48. So the same demographics, the same kind of clinical picture, the same blood clot, same time frame, one to two weeks after the Johnson & Johnson vaccine. Also, the Johnson & Johnson vaccine and the AstraZeneca vaccine are both adenovirus vaccines. So they're similar. They're not the same. The J&J is a human adenovirus, AstraZeneca is a chimpanzee adenovirus, but they're both modified adenoviruses. They took that virus, they weakened it, they made it produce the protein from the COVID virus. So the immune system...

B: It's old school. It's not mRNA.

S: Right. It's old school. These are both old school.

B: Ah, sure.

S: But fine. They're perfectly cromulent vaccines.

B: I was worried for mRNA, though, so I'm not worried anymore.

S: No, no, no. The two mRNA vaccines are kicking ass. I mean, they have the highest...

B: It's the future, baby. It's the future.

S: They have incredibly high efficacy. They're incredibly safe. There's been no problem... Just to be absolutely clear, like the Moderna and Pfizer vaccines, there are no problems with them. 100 million doses and more in the U.S., and there's really no issues, and they've been out longer than the Johnson & Johnson vaccine.

C: But to be clear, with the J&J vaccine, we are seeing... It's a very, very, very, very, very, very, very rare.

B: One in a million.

S: Yeah, so the numbers are similar to the AstraZeneca vaccine in sort of order of magnitude. So there have been, with almost seven million doses, there have been six cases of the clot, one death. So that's a million to one of developing the clot, and seven to a million to one of dying from it. Although...

C: And all in youngish women?

S: All in women 18 to 48, 100% in women 18 to 48.

C: Here's my concern, and this comes up because earlier today, on my 900th job, because apparently I'm not doing enough, I also do a live daily hit for my local PBS station every day. And our reporters today covered the fact that Governor Newsom has decided to suspend use here in California. And I think we're starting to see this across a lot of nations, right? And it's like, okay, well, we've got enough other vaccines, we're probably okay. We know that kids can only take the Pfizer one, 16, 17-year-olds can only take the Pfizer one, so we're covered there. But the concern is that we have such a large population of unhoused individuals, and the one-shot vaccine is so important for public health. And to completely suspend it, even though the vast majority of individuals who'd be receiving it are older and men, it worries me that those people might not end up getting the coverage that they need because they might be hard to track down for a second dose.

E: So why can't they just order a limitation on who can receive the Johnson vaccine?

S: To be clear...

C: I think it's that much more complicated.

S: Hang on, to be clear, the CDC and the FDA presented a joint statement where they recommended pausing the vaccine. The FDA did not pull its emergency use authorization, they didn't ban it, they didn't stop it, they basically left it up to the states with their recommendation of pausing until they have a chance of investigating these reports. And so the states can do what they feel is necessary depending on how their vaccine rollout is going. So you're correct. So one sort of niche for this vaccine, the J&J vaccine, are the poor because they, as you say, think it's a one-shot vaccine, it's easier for that to happen than to schedule two shots. It also doesn't need the cold chain, you can refrigerate it for rural areas, it's better for rural areas.

C: It's just more convenient. It's way more convenient.

S: Absolutely. However, this is complicated. If you look at the big picture, it's less than five percent of the total doses given have been J&J. So it's a very tiny part of America's vaccine rollout. The other thing is there was a huge problem, they tried to shift their manufacture to Baltimore, to the United States, I think it was in the Dutch factories making it, and there was a problem with contamination and millions of doses had to be thrown away. So we're actually in the middle of a shortage of J&J vaccine right when this happened. So already people were not able to get the J&J vaccine, so that's interesting just coincidence. And if you crunch the numbers, I know there might be subpopulations that this could affect, but if you look at the numbers, between the Moderna and the Pfizer vaccines, they are putting out enough vaccines, more than three million a day, to keep up with our ability to get shots in people's arms and to keep up with demand. So this is probably not going to delay.

C: It seems like here in California, the demand is fine, the issue is are there people who we won't be able to reach? And would we have been able to if we had a single shot vaccine available to us?

S: So you have to factor all this together. And again, if you run the calculation, those seven million people who got the J&J vaccine, that saved thousands of lives compared to one person who died from the side effects. So risk versus benefit is on the favor of giving the vaccine, and we do this all the time. The FDA will approve a drug that has a one in a million death toll, that's not a deal killer for a drug, you just get a black box warning. And then they wanted physicians to be fully aware of the side effect that you don't treat it like you normally treat blood clots, they wanted patients to report symptoms. So this is partly for public awareness, it's partly for transparency, and each state has to make a decision about whether or not what the risk versus benefit is. I do unfortunately think that this is going to lead to increased vaccine hesitancy, but it was going to do that no matter how they handled it. Just the mere fact of it was going to do that no matter how they handled it.

E: Yeah, it's very tough to do this right PR wise.

S: So you have to kind of spin it, you have to say, well, this is proof that the system is working, we have a very careful monitoring system in place, it picked this up with very few numbers, we're being very cautious, this vaccine hasn't been out nearly as long as Pfizer or Moderna. And so that those two vaccines have had many more doses over a longer period of time with nothing showing, no red flags cropping up. So the system is working and your faith in the system should be pretty high. And we could quibble about this decision, because it's a hard one, and there are people who are praising the decision and people who are criticizing it for the reasons that we just reviewed, because it's a no-win scenario, so it's just got to pick the lesser of two evils here. They did the best job they could, I think, in terms of making decisions. Again, you could argue that, but again, they didn't pull it, just to be clear, they just made a recommendation of pausing it, the states are deciding whether or not to pause it. And I think that, and most states are, but like in Connecticut, we don't need the J&J vaccine, we're doing fine with the other two, and it's not going to delay anyone getting a vaccine who wants it at all. So for states like that, fine, and definitely there's no downside to pausing it. But in rural states and poor states, it may cause some delays.

J: Isn't the downside that the people whose lives would have been saved, that's not going to happen?

S: What I'm saying is, in a state where they can just substitute Moderna and Pfizer with no delay in vaccination, then you avoid that. In states where you can't do that, they have to think very carefully about how much of a delay it's going to cause.

J: Right, okay.

S: That's what I'm saying. You're right, in states where that matters. But again, there are definitely some states where they have plenty of Pfizer and Moderna vaccine, and some of them are even saying, if you were scheduled to get a J&J vaccine, they'll give you a Moderna vaccine. Just show up and you'll get your vaccine. There's no delay.

B: Awesome.

C: Well, and in a lot of places, you can't even choose.

S: Well, yeah, but I'm saying if you were already scheduled for the J&J, they don't even have to reschedule you. They'll just give you a different vaccine. Yeah. But sometimes some states have to reschedule, and we'll see. We'll see how it plays out in every state. It's unfortunate, but it's not, hey, think of how many different vaccines we cranked out in a year?

E: Oh, yeah.

S: When you study it in 10, 20, 30, 40,000 people, and then you give it to millions, of course things are going to crop up when you give it to millions. What's going to crop up are these rare things that happen one in a million. You're not going to see a one in a million side effect when you study 40,000 people. This is, there's no way to avoid this. That's why we have the monitoring system that we do to pick this up when it happens. I also think the FDA said they're acting out of an abundance of caution. I wonder how much they adjusted their standard operating procedure to the fact that we're in the middle of a pandemic. You know what I mean? Because if there was not a pandemic, this is a no-brainer. This is easy. You pause it. You collect the data. You study it. Pausing it can cost thousands of lives. Then the calculation is different. Just like with the European countries, they made a bunch of different decisions. I think the UK nailed it where they didn't pause it. They waited for the data, and then once it came in, they said, all right, we're not going to give this to young women or people who are low risk for COVID. We're going to just give it to older populations. They kind of slipped right into, I think, what the best risk management scenario that there is. But anyway, we're totally Monday morning quarterbacking all of this, absolutely. But hey.

C: Yeah, we have all that.

E: Best we can do.

C: I mean, we still don't actually have all the information, and that's the interesting thing about this unrolling in real time.

B: Steve, I heard that they were going to have a big meeting today and really talk about... Did anything come out of that specific meeting today?

S: I haven't seen it. I think they were going to start meeting today. I don't know if they were going to issue statements today. Probably later this week or early next week, I would expect. I mean, they're definitely fast tracking it. So more cases are going to come forward just because of underreporting, but also there are people who are still in the window. They got their vaccine three days ago, and they're still in that two week window. So there definitely will be more cases. The current count is an underreport. But it's still going to be, I think, similar to what we're seeing now. Single digits per million people vaccinated. But the other thing is, and when I wrote about this in Science-Based Medicine, this is sort of my conclusion. It's like, yeah, this is unfortunate, but it's par for the course. This is what it's like to roll out new medications, and we monitor them, and we respond appropriately. Everything is playing out exactly as it should when you really think about it. The real vulnerability is the epidemic, the pandemic of misinformation that's out there, and the fact that this is happening on a background of an anti-vaccine misinformation campaign playing out over social media. And so they're really causing a lot of havoc. And that is a vulnerability for our society. We talked about this last week, and I want to get into it again, but we've got to deal with that. We have to deal with it.

C: Absolutely. Yeah. If we're already struggling with distrust, and then something that we totally expected could have potentially happened, happens, but we communicate it or we telegraph it poorly, then in many ways, simply how we contextualize this can contribute to that distrust, so we have to be very careful.

S: Yeah. I mean, the challenge is we need seven and a half billion people to all make rational decisions at the same time.

C: Exactly.

E: And it's just no problem.

S: Yeah, it's hard.

E: We'll need a day or two.

S: It's a high bar.

C: Do we have any sort of good evidence yet based on the growing numbers and these more controlled places like college campuses or closed places of where herd immunity looks like it needs to net out?

S: What I do know, you actually read a study today, but of course, this data is always months behind by the time the data gets collected, analysed, published, is that so far, so far that we could tell that social distancing and mask wearing is having a greater impact than herd immunity, so the herd immunity piece hasn't kicked in yet.

C: So we're not quite there yet in terms of the percentage.

S: But the data is, of course, lagging behind the reality and the ground. We probably won't know that we're there until six weeks after we are. You know what I mean?

C: Well, and even as of today, aren't we only like 25% or something fully vaccinated?

S: Fully vaccinated?

C: Yeah, fully. I think it's still pretty low, like I wouldn't think herd immunity would be, we'd be anywhere close to it quite yet. I'm just wondering based on modeling, where do we need to be? Is it 80%? Is it 60%? Is it 90%?

S: We don't know. We don't know that number. We'll know that number in retrospect.

C: When we get to it.

B: I've heard 80%, but we'll see.

S: That's a good, it's a good guesstimate, but we don't really know. And unfortunately, if you look at the number of new cases per day, it's starting to turn back up.

C: Yeah, I've seen that, especially in like specific pockets as well.

S: Yeah, we're not out of this yet.

B: Now that millions of people have it, we're seeing something. What happens when we get over a billion people get the vaccine? You think anybody could be like a superhero? Too soon?

S: What's the billion to one reaction? Superpowers? Maybe that's what we should tell people. Hey, one person in a billion is going to be getting superpowers.

E: Make it a lottery.

C: Don't miss out on your chance.

E: That's right.

C: You could be the one.

E: Can't win if you don't get inoculated.

J: Yeah, but then people will get it multiple times.

J: Oh my god. Oh damn.

S: Now we have to tell them that that will undo it if you get it.

E: Oh, that's right.

S: The vaccine will nullify your chance of getting it.

B: Gives you evil superpowers.

E: Oh, more. I mean.

News Items[edit]

Possible New Force (16:38)[edit]

S: All right. Well, me and Bob, we have some really exciting news. I'm just talking about this week. You're going to start us off with the possibility of a new particle or force.

E: No way.

B: Yeah, this is over. This is everywhere. I've seen this so many times. Definitely had to talk about this. So potentially big or at least very interesting news from the world of particle physics this past week. Particles called muons have been observed behaving in a way not predicted by the incredibly successful standard model of physics, which you've talked about a lot on the show. Does this mean finally that there's a major update for physics, a major cool new discoveries or perhaps is this just a minor tweak or is this probably nothing? So what's going on? So this comes from Fermilab's long awaited experiments on muons and recently published in the journal Physical Review Letters. Now at a high level, what's happened is scientists have accelerated muons in a magnetic field and the high precision measurements confirm and extend the and greatly refine previous measurements that don't agree with theory. The superficial excitement here, of course, is that this could portend to new physics that could finally give some insights into some of physics biggest mysteries, dark energy, dark matter, combining general relativity and quantum mechanics. I mean, who knows? I mean, that's best case scenarios are very, very exciting. First of all, though, I would like to congratulate the hundreds of scientists all over the world who collaborated on this extraordinary feat. And like for decades, they've been working on this, literally, they've been working on this specific outcome for since the 1990s measuring muons in this way. And it really was a tour de force of awesomeness. So regardless of what happens, bravo, brava to all the men and women who have worked on this. So what are the facts? More specifically, what the hell is a muon? And is it called a muon? Or is it a muon? I think it's pronounced muon. A lot of scientists I listened to the past few days are saying muon. So I will say that.

E: Is that because of the Greek letter mu?

B: Yeah. And so, yeah, so I've been calling it muon for God knows how long, but oh well.

S: So muon?

C: Muon.

S: Oh, muon.

B: Yes.

C: Muon. Like mew, mew, mew.

B: So you can think of a muon as essentially a corpulent cousin of an electron. Same thing, but just more massive, like over 200 times as massive. They are truly elementary particles, meaning that there is no internal structure. It's a point particle, unlike an atom or even a proton. They all have internal structure. There's also a third cousin as well, and he or she is called tau. And that's even more massive. She's the most corpulent-licious version of these bad boys. And together they are leptons. They are part of the family of leptons. You may have heard of that. Leptons are fascinating. So there's three. Electron, muon, and tau. And those are the charged leptons. There's three others and they are uncharged. Can you guess what they are? Yes, Bob, you are right. They are the neutrinos. Neutrinos are leptons and very distant third or fourth cousins to electrons and muons and tau particles. And, of course, to fill out the lepton family, you've got to throw in the antiparticles because they're in there. They're in there as well. So now you're probably wondering, well, if these other electron cousins could orbit atoms, like the normal electrons, is that real? Does that happen? Yes, they can. You can have an atom with a tau or muon orbiting instead of a regular electron, but these are exotic atoms, but they are very short-lived. Muons and taus are unstable. They decay into electrons, which fortunately are extremely stable. But yeah, any cool atoms like that, if they are created, don't last beyond microseconds. So that's unfortunate. Or maybe it's fortunate because who knows what kind of weird universe we live in with exotic atoms everywhere. So, okay, kids, it's time to put on our imagination hats. If you want a mental image, think of a muon as a tiny ball of charge that's spinning. And a spinning charge like this behaves very much like a common bar magnet, a straight piece of metal with a red north and a white south on the bottom. I haven't seen one of those in a few dog's ages. Now remember, though, mental images like these can definitely help, but remember, these are imperfect mental analogies, but that's probably the best our baseline human minds can do right now. So, okay, so this is player one. The muon is player number one in this experiment. Muons have a magnetic field and angular momentum. And our limited minds can think of that as spin, like it's often compared to a spinning top or a gyroscope. That's a good way to think about it. See, then after player one, now we've got player number two. And in this experiment, player number two is an intensely controlled external magnetic field that is exposed to and surrounds the muon. So these two guys are kind of like in the same space. The muon with its magnetic field and this external magnetic field. Now when you have, when you introduce this external magnetic field, it causes the two magnetic fields to interact, and that causes the muon spin to process. The spin axis processes, and that's roughly, procession is roughly analogous, again, to the axis of a spinning top moving how it moves in circles. The ends of the axis move in circles. That's a good way to think about it. And it's this procession that is the focus of this experiment. And it's this value that is called the g factor. And that this is what they're trying to calculate or trying to use this, this procession to infer the very extremely precise value of the of the magnetic moment of this muon. So yes, the speed of that procession tells us precisely how strong the muon's magnetic field is. We can then measure the strength and compare it to theory to see if they match. And if they match, then the theory is correct. And that's awesome. We have confirmation of this amazing theory yet again, more confirmation. But if it doesn't match, we may have some new physics. So it's always an interesting possibility. Now there is a third player here making this kind of like a quantum threesome. And these are called virtual particles. We've mentioned this on the show, and I love virtual particles. We know that a vacuum is anything but empty, right? You think the vacuum is the epitome of emptiness. No, not at all. All sorts of particles appear from apparently nothing. But really, it's really they're appearing from the energy inheritance space time itself. They disappear and they appear and disappear too quickly for the universe to really care. But also, some of these particles, some of these virtual particles we can't make in any collider that we have on any drawing board. They are just like too massive. They exist for such a brief period of time, we really can't directly examine them, which is unfortunate, but we can investigate them indirectly.

E: How do they exist in nature then?

B: At the quantum level, these virtual particles appear out of nowhere. They kind of you can have a particle and antiparticle appear out of nowhere and then hit each other and annihilate and disappear. So yeah, they pop in and out of existence and they interact. They can interact with particles and this is what's so important in this context. So these virtual particles surround muons. If you could look at a muon, you would just see them all over the place. And they can interact with the muon and have an impact on this G factor. So we have to take that into account. Okay. So all right. We have muons which are revealing to us the exact strength of its magnetic field because of the way an external magnetic field and virtual particles affect its procession. That's the big picture of this.

S: Bob, do you know what subatomic cows say?

B: Muons. Good one, Steve. Okay.

E: We were all thinking that.

B: So now the standard model though just laughs at all this complexity. It takes into account all of this and predicts a very, very, very specific value for the G factor and it's called G minus two, which is actually the name of this entire experiment. The accuracy of the prediction in the standard model is 400 parts per billion. Very, very accurate. Now the Fermilab Muon G2 experiment is designed to be accurate to only 150 parts per billion. That's like measuring a football field accurate to a tenth the width of the iconic human hair that's always used in these comparisons. So amazingly accurate. When this initial measurement from Fermilab is compared to theory, it does not match. And this is exciting obviously because it means that there could be some unknown virtual particle that smacked the muon in the face and changed its procession in a way that an amazingly accurate landmark theory knows nothing about it. So that's why this has so much potential because this is something that the standard model just has not predicted. So this is why this could be something tiny and insignificant in some ways, but it also could be the other end of the spectrum, something huge and amazing. Fermilab physicist Chris Polly told the New York Times, this is our Mars rover landing moment and Rene Fatemi is a physicist at the University of Kentucky and is also a simulation manager for the Muon G minus two experiment said recently that this is strong evidence that the muon is sensitive to something that is not in our best theory. That's a really good way to put it. And I can't disagree with these scientists, mainly because I'm stupid compared to them, but I can put this in a context that could be that you may find interesting. So as usual, it's premature to celebrate. Do not break out the bubbly for this. I mean, you could do it just for the raw accomplishment itself, but don't start, don't pull out your new particle/new force bubbly. I'm going to wait on that. And that's mainly because of our buddy called Sigma. We've mentioned that on the show many times, experiments, anything that has experiments typically will use Sigma to measure standard deviation, right? And that's used to express how likely is a result. Is it just random chance or what? And the Sigma can really help us wrap our head around it. Now Brookhaven National Laboratory did the very first experiments with G minus two in 2001. I mean, two decades ago, and they found this G factor anomaly. They found this difference between observation and theory. And they calculated Sigma at 3.7, which is it's okay, not anywhere near the gold standard of five Sigma. Now the first result from Fermilab, the thing that we're talking about right now, this is the first result, the initial result from Fermilab that combines with the Brookhaven because they're using most of the same equipment they're using. They actually transported the entire ring to Fermilab. So when you combine the Fermilab results with Brookhaven, it brings it up to 4.2. Now that's 99.7% probably accurate. There's a 97.7% chance that this is real and not just bad luck one in 40,000. That's good, right? That's good. One in 40,000, but that's still nowhere near the gold standard, which is five Sigma. That's one in 3.5 million. So if you're not at five Sigma and you're making a huge claim, well, I'm sorry, talk to me when you get to five Sigma because we cannot assume that this is right even though there's only a one in 40,000 chance that it was a coincidence.

S: But Bob, let me point out at this point, though, that this assumes that there's no experimental error, right? This is just, if the data is correct, what's the probability that this data was occurred by chance alone, one in 40,000, one in 3.5 million. But this has nothing about there being some systematic error in the experimental setup or the way they're measuring things. So like, for example, I believe if you remember like the faster than light neutrinos, they were up to six Sigma with that. But that doesn't matter because they had a bad cable the Sigma doesn't account for things like, you know.

E: Yeah, are they trying to falsify the hell out of this thing?

S: A hardware problem. So it's not just that when we hit five Sigma, it's proven. We also need to replicate this with different equipment in different labs to know that there isn't some systematic problem there.

B: Right, right. And that's definitely part of the process. And that kind of relates to my next quote by Bruce Shum, he's a professor of physics and he's the author of a popular book on the standard model itself. He said, there's a little bit of skepticism that's been cast on it. When you make a measurement and you compare the expectation based on everything we know, the standard model, there's a little bit of concern that maybe the calculation wasn't done quite right. And yes, the standard model has been amazingly almost unparalleled how successful it's been over decades. I mean, it basically lays out all of the forces and particles that we are aware of in physics and its predictions. I mean, we found the Higgs boson based on purely on theory, on the predictions of the standard model. We knew that it had to be around this energy regime and we found it at the LHC purely because of the standard model. So when you tell me, when you come to me and say, hey, it looks like the standard model got this one bit wrong, and we're at 4.2 sigma, it's like, well, okay, that's great. But you know, chances are, there's probably been a mistake. That's what you got to assume at this point. And sure, look really hard and bring up sigma as high as you can. But until that, until sigma gets really good, then you can't really make too many assumptions because standard models is too amazingly successful to think that it's made some big mistakes here or that there's such an important chunk of it is not there regarding these types of particles and forces. And don't forget, though, Steve, Fermilab has gone over 6% of its experimental results. What we are talking about today is because of its 6% of what it's gone over. So we're going to have to wait a couple of years before it analyses all the data. And maybe they'll shoot what you know, maybe they'll hit five sigma, maybe they'll go to six, who knows, but we're going to have to wait until until that happens. If they do get over well over five sigma, and they still and they could replicate it and all that good and we say, yep, this looks we have to think that this is real, then then that of course, that would be fantastic. And as my my smart friend Leonard Tremille says, he's recently described, he said, when an experiment overturns theory, and that does happen, it has happened in the past, an experiment actually overturns a theory that usually leads to a couple of possibilities. In this case, the overwhelming likelihood is that the standard model would be tweaked, but essentially remains the same. And that would be kind of like a disappointment. But you know, this is what I'm expecting to happen, that they're going to find that you're going to find this particle and force and that a new force, that's a reason to get drunk right there. You find a new particle and force like this, absolutely start drinking. That's wonderful. I mean, Cara will be telling her kids when she's in 80s, like I remember when Bob first talked about this on the show. Absolutely. And that would be great. But there's a much less likely but a very real possibility that this opens up whole new concepts and models for physicists to use to potentially explain things that the standard model definitely cannot deal with, like gravity, like dark matter and how Jay's meatballs can taste so damn good. The standard model goes nowhere near as any of that stuff. And so there's definitely gaps in the standard model that we need theories for that we don't have. So those are the kinds of theories. Those are the kinds of breakthroughs worth waiting for. So keep your eye on this one.

E: Jay's secret ingredient is muons.

B: Muon balls.

S: Yeah. So, I mean, I wouldn't be surprised if we learned that there was some kind of experimental error, a calculation error, like the sort of the way that they're calculating or measuring the result is off. Because this is tricky.

E: Because it's happened before.

S: And it's happened so many times before that that's a good first assumption. And then if this is real, I think it's most likely that we're going to get a tweak to the standard model. But the same model is correct as far as it goes, but it's missing a little piece. And I think the major change in fundamental physics is the least like the outcome here. But of course, that would be the most exciting.

B: And it's still possible. And don't forget, this isn't the first experiment. This is a follow up on the Brookhaven experiment from 2001. And this just refined it and made much more refined results, much better results, still pointing to this anomaly. So that's so that's kind of like a second confirmation here.

S: Well, that's all exciting, Bob. But I think I may be able to outdo you.

B: Try.

CRISPRoff (33:45)[edit]

S: So we've been talking about CRISPR for a long time now.

C: CRISPR.

S: CRISPR. So CRISPR was actually discovered when? When do you think that?

J: Ten years ago.

E: 2005?

C: Yeah, five to ten.

B: It's in the odds.

S: Ninety three.

E: Ninety three?

B: Really? That first paper came out in the early 90s, huh?

S: Yeah.

B: Wow.

C: But we're talking about the technique.

E: That's 14 years before the iPhone.

C: Yeah, but obviously it wasn't being utilized the way it's being utilized.

B: No, the birth of the worldwide web.

S: So in 2013, that's when they figured out how to use the CRISPR-Cas9 system as for gene editing. That's what you guys are thinking of. But really, that was 20 years after the discovery of CRISPR, which is that's how things work in science, right? The basic science is usually some cool application comes decades later. And CRISPR, which stands for.

E: We've been through that before.

S: Clustered regularly interspaced short palindromic repeats.

C: Repeats! I picked up the Rs. Damn it.

B: I just memorized a goddamn acronym yesterday. I looked at it.

S: It's hard to keep in your head.

B: I don't want to forget this. I don't want to forget this the next time Steve asks.

S: But which is which is we had so we had recombinant DNA technology in the 70s, 80s. And then in the 80s, we discovered the zinc fingers. And that was that was the first programmable.

E: Jay, put my zinc finger.

S: That was the first programmable sort of genetic modification. But it takes a long time to do. It's expensive. And then in 2011, there was Talon, which was faster and cheaper. And then it got eclipsed by CRISPR in 2013, which is much faster and cheaper. And that's really what revolutionized programmable gene editing, because you have the CRISPR itself, which is a way you can compare that. You can pair that with an RNA targeting sequence. And the CRISPR can find and match that sequence of DNA. So you could say, I want to go to the part of the DNA that has this sequence in it, and the CRISPR will go there. And it can also deliver a payload. The Cas9 is the payload. And what that does is it makes a double it make it cuts both strands of the DNA. And so we can use that to knock in or knock out genes. You know, the knock out means you make it so that the gene doesn't function. Knock in means you're adding a gene that you want to be functional. Knocking out is a lot easier. All you got to do is make that double stranded cut. And then the most common natural repair mechanism called non homologous end joining or NHEJ will put the two ends together, but usually in such a way that the gene no longer functions because it makes some kind of a frame shift where the code gets scrambled. At the at that area where it was cut.

B: Yeah, I never realized that, Steve, because CRISPR does the hard work of cutting. And then it just like walks away and it's like, yeah, yeah, the maid will clean this up.

S: Yeah, let's the cells own repair mechanisms take over. If you want to knock in a gene, however, you have to use the much less common form of cellular repair. That's a lot slower. But this is the homology directed repair HDR. And that, if you do it correctly, can maintain the structure of the gene so that it will still function. That's more complicated to pull off. But with CRISPR, you have targeted a programmable targeted way of either knocking out or knocking in a gene wherever you want in the DNA. Obviously, there could be off target changes. We always talk about that. That's not perfect. Researchers have learned how to sort of dial up and dial down the speed and specificity of CRISPR. So we're sort of really learning. We're still on the steep part of the curve. We're really learning how to control it a lot better. Well, all right. Now comes to well, a pretty significant advance in CRISPR technology, pairing CRISPR with a new payload. This is a single dead Cas9 fusion protein, whatever that means. That's the payload now. And this doesn't cut the DNA. It doesn't change the DNA at all in fact, what it does is methylate the DNA.

B: Yes, methylate, baby.

S: Yeah, it adds methyl groups to the base pairs. And this is a natural mechanism that is used, like an epigenetic change that that can affect transcription. So the methyl groups basically get in the way of the transcriptase enzyme so that it's not able physically to turn that DNA into into a protein.

C: Right. But it's reversible, right?

S: Into an mRNA and then into a protein. But yeah, but since it doesn't alter the sequence of the DNA, it's reversible because the structure of the gene is intact. So so what does this mean? It means you can use CRISPR with this with the single dead Cas9 fusion protein, which they're calling CRISPR off. You can do that to turn off a gene. I want to turn this gene off, methylate it and turn it off. Now, going into the research, which established that the effectiveness that the CRISPR off works, the assumption was that this would only work in about a third of the genes. Because there's something called canonical CPG islands.

B: Like dead zones? Yeah. Yeah. Yeah. The islands.

S: The canonicals are CGI's and the CGI's are where the methylation happens normally. So they figured, OK, so it's only going to work on the third or so of genes that have these CGI's. But when they did the study, they found that, no, it works on almost every gene. It's not limited. It's not limited to the to the CGI's.

B: They got drunk that night.

E: I don't understand, Steve. Why did they think they would only work on a on a fraction of them? Because previous evidence suggested that this methylation process only works on genes that contain these CGI's. So this is just based on previous research. So this this basically contradicts that previous research, which means that what we thought was true about CGI's isn't true. They're not necessary for methylation to work. And therefore, this methylation CRISPR off technique works on almost all the genes that they tested.

B: Why almost though? Is there a little holdout of a few percent?

S: Yeah, it's not 100 percent. It doesn't work. They didn't work every single time, but basically on most genes.

E: So we can turn off some pretty nasty stuff.

S: Well, we'll get to the applications in a moment, but potentially, yes. The other thing they found was they didn't know how long this was going to last. Maybe it would last just in the cell that they did it to. But in the the the descendant cells, if that cell copies itself, the copies would would revert back to the un-methylated, active gene state. And what they found is, no, it persists pretty much as long as they studied it. It's semi-permanent.

B: Talk about a best case scenario.

C: Did they do this in somatic and germline cells?

S: So that I don't know if they did in germline cells.

J: So when you say that, Steve, it means that they make a change and the change stays forever.

'S: As long as they've said, as long as they've looked at it.

C: Yeah, forever is strong. Because if it is an epigenetic phenomenon, it's very likely that it would go away eventually.

S: Yeah, exactly.

C: But through are multiple rounds of division it's sticking around.

S: Yeah, exactly.

C: That's cool. That's really cool.

S: So that makes it really useful, right?

C: And the truth is, if it does go away, you just do it again.

S: Yeah, but it doesn't go away immediately. It lasts for quite a long time. So this means that you can cause reversible turning off of a gene that it pretty much applies to almost any gene and persists for a long time. And they made CRISPR on to turn the gene back on. So now we have an on off switch.

C: That's awesome.

B: Is that incredible or what?

S: Yeah. Now my question is, how incredible is this? Why is that? Why are we getting so excited about this? So first of all, for just genetic research-

B: Superheroes, hello.

S: Well, for genetic research itself, the ability to cheaply, quickly, semi permanently and reversibly turn off and on genes is a huge boon.

B: Holy grail.

C: Oh, yeah. This is instead of breeding an animal that knocked out animal and then like having to rear the animal and then do experiments with it. You can just knock out the gene in in a fully function. I mean, that's amazing. Then you can have these perfect control groups right next to them. I mean, everything about this changes the game.

B: Oh, my God.

S: This is rocket fuel for genetics research. And this is why our knowledge of genetics has really been taking off in the last 20, 30, 40 years, because our knowledge of genetics is improving the technology of genetics research. This is a great example of that. So there's a positive feedback loop in genetic research. That's why sequencing a genome today is thousands of times cheaper and faster than it was 30 years ago. It's like computer transistor progress level. It's geometric. It's not linear. So it's absolutely amazing. All right. But what about clinical applications?

B: Bring it. So let's hear it.

S: Well, so this has exciting possibilities. But it but this is tangential to it doesn't solve the biggest limiting factor with with clinical applications of CRISPR, which is how do we get the CRISPR into their cells we want to get them into. We still need a vector. So it's this is great if you're doing in-vitro fertilization and you want to alter the genome of the embryo. That's great. Or if you're doing it in a cell line in a Petri dish for research. Fantastic.

C: Because then you can just inject it.

S: Yeah, exactly. And if you want to do it on something in the blood or the bone marrow or something where we can get access to it very easily.

C: Yeah, maybe in your eye or.

S: Yeah, exactly. Vitreous humor of the eye. You can inject it there. We can inject it into your spinal fluid. We can take your blood out, do it to your blood, put your blood back in. We could do the same thing for your bone marrow. So anything like that. But for your liver, like we can't take your liver out, CRISPR it up and put it back in.

C: Right. Your brain.

J: We can take it out, though.

S: For solid organs, for solid organs, we just don't have a really good way of getting CRISPR to the cells we want to get them to. So that vector problem is still a huge limiting factor on all the exciting clinical applications for this. But we're working on that. But remember, in the 1990s, we were we had a vector problem with with with gene therapy. This is pre CRISPR.

B: Cause of death.

S: Retroviruses.

B: Remember that kid died.

S: Yeah, exactly. We ran into problems there. And it took 20, 25 years to sort of get to the same point, where we were then to sort of to fix these hurdles. So it's really hard to predict like how much of a hurdle this is going to be. We may solve it tomorrow or it may be 30 years now. I'll be like, oh, we're still waiting for that CRISPR, you know.

C: And the distinction needs to be made between treating a child or an adult who has a genetic disease and preventing genetic disease in an embryo. And that's where a lot of the ethical questions come in.

S: Yeah. Yeah.

C: Because it's much easier to. I mean, not easier. But the vector problem is less of a problem if we're talking about putting it into an embryo.

S: Totally.

C: Or putting it into a single fertilized cell.

S: It's not an issue at all. Yeah, that Chinese scientist, Dr. He, I always forget which one of this. I think Dr. He. He did it. He did it right. He's done. So that's not a problem. It's it's getting it into an adult. You know, you have an adult who has a pancreas problem. We want to fix your diabetes in your pancreas. How are we going to get the CRISPR into your pancreatic islet cells? You know, that's what we need to figure out, for example. And that's tricky. And so that's we're still waiting on that. When that breakthrough happens, then then the gloves are off on CRISPR. Then it's incredible.

C: Because then it reaches every aspect of medicine.

S: Totally.

C: Literally. I mean, it revolutionizes drugs.

S: So, for example, for example, they're already talking about, like, as one potential application, Alzheimer's disease, part of which is overproducing tau protein. Well, we can turn the tau protein off, CRISPR off. No worries. We just need to get the CRISPR to your all your brain cells. I wonder if like if we just put a lot of it in the spinal fluid, if enough of it will get to the surface of the brain to that, it would be if I don't know.

C: Or maybe it's worth it to open up the skull?

S: Well, you can inject it into your, you could just stick a needle through. You just put it into your, you know. So, yeah we'll see. I mean, I wouldn't again, if you're somebody who's slowly degenerating from Alzheimer's disease, that justifies aggressive research. So I wonder how long it will be before we start seeing some research there. But again, we just don't know how well it's going to penetrate, how many of the cells it's going to get to and how clinically effective that's going to be. So there's still years, probably decades of research ahead of us. But this is really exciting potential.

C: Yeah. It's sort of like my concern not to put a wet blanket on it because it's so exciting. And again, it's almost like the way that gravitational waves are revolution. It's a new type of astronomy. This is like a new type of intervention. It's different than drugs. And when you think about drugs as an entire class, all drugs is a type of intervention. I mean, think about how the multitude of drugs that exist and how many lives they've changed.

E: Powerful tool.

C: It's huge. But the thing that worries me-

S: It's epigenetic therapy. That's how cool is that?

C: It's so cool. I think the thing that I'm most concerned about when I to temper my excitement a little bit, just so I don't get overly, overly excited, is that much like cancer, there are certain situations in which unless you get them all, they just keep coming back. And my concern would be about treating some sort of genetic, whether you're turning off an expression or you're turning on an expression, if you can't get to all the cells or you can't get to a certain number of the cells, does it just are we just chasing our tail over and over?

S: So that is clearly going to be an issue disease by disease. But I'll tell you, Cara, I think that just my general medical knowledge that so many things that the negative clinical effects come in when you start to affect 60, 70, 80 percent of the cells.

C: That's so good to hear. It's like a herd immunity.

S: You lose 70 percent of your kidney function, and then you start to notice kidney disease. There's a lot of reserve built in to so many parts of your body. Like you could lose a lot of your liver and be fine.

C: Something like Alzheimer's, where it's cumulative. It builds up. The proteins build up over time.

S: Exactly. So slowing that down would slow down the progression of the disease. And may be so much that because it progresses over decades. If you slow it down so that you're probably going to die of something else before it becomes significant.

C: And we see that with targeted cancer treatments. Now, when we have a molecular marker on a tumor and we're able to treat with a targeted oral chemotherapy, a pill as opposed to radiation or intense chemotherapy, that's sort of not as targeted. We see people who have metastatic cancer living for decades, certain types, because they're able to keep the tumors at bay. It doesn't mean they go away all the way. But if they can keep them under a certain threshold.

S: Yeah, they're not cured, but they're in remission to the point that that's not what they're going to die from.

C: Yeah, they're just carrying the disease. They're keeping the disease in check.

S: So a lot of things like when I think of the diseases and what I know about them, most of them would respond very well to this kind of treatment, even though it's partial. It would have a significant effect, even like sickle cell. You don't need to make every single blood cell normal. You just need enough of them to be normal that you don't go into a sickle cell crisis.

C: Well, can you imagine like the mental health applications to like expressing more or less of a neurotransmitter? I mean, there's so much cool stuff here.

B: Imagine how about this? Imagine you get this deployed somehow to every cell in your body. Just waiting, just waiting for you to tweak it, to methylate some genes.

C: But you have to do that. It's still targeted. You have to tell it what to methylate.

B: I know. I'm assuming I'm assuming we've we've solved the problem of delivery. And then you have an app, you get an app and you say, I want this. I want to deactivate this gene and soup up this gene. Do you activate that one?

C: See, when you go to your techno-optimist place, I get horrified. And I'm like, no, we don't want this. We don't want this.

E: It is a moment to pause.

J: Steve, what do you think would be the early applications?

S: Well, in research, this is going to be used for research first. Absolutely. Clinical, I think, will be, again, things where CRISPR can target the tissue, like in the blood and whatnot.

C: And also probably like severe life threatening, like cystic fibrosis, like these very specific types of diseases, right? That's where we're going to see research applications.

S: For cancer, what if we can get enough of it into the cancer that it turns off the cancer mutations? You're no longer a cancer cell, you know?

C: I know. Yeah. I mean, it would be insane. I mean, I just think of all the like, especially all the genetic diseases that we know are a simple switch. It's like my body produces too much of this one single gene. Yeah. Like those are, oh, my God, like phenyl ketoneuria. I don't know if that's single gene, but it's like it's such a specific thing. It's like just I turn this one compound into another compound and that builds up. So if I can just stop doing that or I can't clear a compound or my liver produces too much of something. Like you look at all of those types of applications and it's just like, it's amazing. It's amazing.

S: It'll be easier for things where we're like for mutations, where you don't produce something, then that would this would not be that would not be as obvious an application. Because this is turning something off, right?

C: Yeah, but they have the on switch now, too.

S: But that's only to turn back on something they turned off.

C: Maybe, but I bet you soon we'll figure out how to turn things on that weren't there, because I bet you it's in your DNA.

S: Not if you have a mutation in a gene and the gene is off, not because it's methylated, it's off because there's a there's a frameshift mutation.

C: You're right.

B: Just to snip it out, but there might be knock it back in.

S: Well, now you're talking about knocking in a gene. That's not CRISPR on off. That's right. That's that's Cas9. That's some other application of CRISPR. Just want to keep things in their lane.

C: Which we already have.

S: Yeah, that's it. They're just different CRISPR applications that we would use in different things. I don't think they would be using this for GMOs, because you want to make permanent genetic changes in a GMO stable GMO line. You don't want to just make epigenetic changes. Although what I said when I was writing about this is like, wouldn't surprise me if they figure out how to make an epigenetic change to make a crop better. And of course, it goes away after a while. So it's like built in patent protection because it's not.

C: Oh, brilliant.

S: But they already have that with hybrid seeds, by the way, before you get all anti-corporate. The hybrid seeds can't be you can't breed them again, because that's only for one generation. Do you get that perfect mix of genes? So this would be the similar kind of thing.

C: But this gives you like a slightly longer lease. I love it.

US Power Half Way to Zero Carbon (54:04)[edit]

S: All right, Jay, this is I've been reading about this. I'm not really sure if this is good news or not, but apparently our carbon emissions are down. Tell us about that.

J: You don't know if it's good news or not?

S: Well, go ahead, tell us what's going on and we'll dig into it.

J: So as climate change becomes more and more of a looming mess around the world, the United States seems to be starting to actually try to get their carbon emissions under control. So so far, 17 states, Washington, D.C. and Puerto Rico have enacted laws that will enable reaching the goal of getting to 100 percent carbon free electricity production over the next two decades. Now, two decades puts us into 2040. And a lot of times you'll hear the date 2050 thrown around as the goal. According to this study, that's 10 years before that 2050 date that has just been thrown around for the last few years. So this is really good news. And it's also supported by historical data that shows that it's definitely possible to have significant reductions in carbon emissions. People just have to do things. The Department of Energy released new research outlining how things have progressed in the last two decades. This is actually goes back to 2005. If no measures were put in place to reduce carbon emissions, there would have been an increase from 2400 to 3000 million metric tons from 2005 to 2020. So that's 2400 to 3000 million metric tons. That was the expected increase. The actual emissions reduced to 1450. So they were saying that we were going to go from 2400 to 3000 in those 15 years. And we actually went down to 1450 million metric tons. That's 52 percent below the projected level that we expected to get to. So this reduction in carbon emissions, it's left a significant impact in different ways. And this is all good. First, the number of jobs in electric electrical power production increased by 29 percent. Of course it did, because look at the explosion of solar panels and wind farms and everything over the last decade and a half. They also saw an 18 percent drop in consumer electricity costs, that's also significant where how come people are using less electricity? We have more electronics now than we ever did. This this resulted in an 86 billion dollar savings per year. So these changes were due to a couple of things, better governmental policy and technological advances, like efficiency as a big factor.

E: LED lights.

J: Right. Exactly. So the the total demand for electricity didn't change much between 2005 and 2020. Back in 2005, they predicted that there would have been a 24% increase in electrical demand by the year 2020, but it never happened. So in part, like I said, this was because of more energy efficient products, advancements in technology and improvement in government policy. In 2020 wind and solar generated 13 times more power than they predicted we would be at in 2005. Now, I can give the version of us in 2005 a break because we didn't realize just how fast the technology was actually going to take off, which is an incredibly huge factor in and how much we've we've purchased into or bought into solar and wind technology. But the technologies have just really exploded. And that's why we're using them much more than we ever thought we were going to. Another significant factor in the report about lowering carbon emissions was moving from coal to natural gas. Now, you might ask, what's the big difference? There's a huge difference.

B: It's a big difference.

J: Because coal is so much more dirty than natural gas. I mean, it watches all the bad porn, the bad stuff. So natural gas is is just a cleaner fuel. That's it. So it's a better way to go. Because less oil products were being burned, there was a reduction in sulfur and nitrogen compounds. This has been incredible because it led to a decrease in respiratory disease and way more impressive is that there were there was a decrease in premature deaths. It dropped from thirty eight thousand to thirty one hundred per year. That's fantastic. Yeah. So apparently if we stop burning poison and stop putting poison into our atmosphere, people live healthier lives.

E: What are you trying to say?

J: Look, I'm not trying to take a positive here. I'm just reporting. But this was a fantastic report. So wind, solar and battery technology are going to have are going to have a significant role in lowering carbon emissions moving forward, many projects are in the works to help get down to zero carbon emitting power sector. But of course, what it's going to take real legitimate vigilance to make sure that it actually happens. We've talked about this on the show many times, but the infrastructure requirements are going to skyrocket in order for us to support having renewables be supplying the vast majority of our power. And again, having electric cars and everything that we want to do, our entire grid has to change. The grid will have to be able to ensure electricity is delivered. Look at what just happened in Texas. They they didn't spend some money to to winterize their windmills and they got smacked with a massive thing. Lots of people lost their lives. Tons of damage to property and everything because they had a cold spell. We have to be willing to spend the money. We also need to build a new transmission infrastructure. The grid itself has to be redone, re-engineered. And this is no small feat. The way that the grid operates will have to be, it's going to have to be incredibly more efficient. We're going to have to have a new management system for the grid. You know, it has to be able to be operated in a different way than it's operated now. You know, we have ways of passing electricity from from place to place and things like that. But we're really going to have to have the grid be intelligent. It has to have a real intelligence behind it. We have to use more nuclear energy, solar thermal, geothermal energy, longer duration energy storage can be could possibly be achieved by using hydrogen, bioenergy, synthetic fuels. I mean, there's all these different things that we can do to not just collect the energy in better ways, but to store it and to have it be on demand. And these have to be the engineers have to get to work. Because this is going to take a Herculean effort in order to to change the grid as quickly and as seamlessly as possible. The past 15 years have clearly shown us that we are terrible at predicting the future. I think I know a couple of people who are writing a book about how bad people are at predicting the future. So what we do know is that technology and governmental policy are essential in order to make these changes happen. Now, the technology, of course, it's happening. The market is making it happen. The market driven demand is always going to push technology forward. Look at cell phones. In summary the technology presented itself about 15 to 20 years ago. We took it and ran. Things have gone extraordinarily well, particularly in in the United States, because this is the report that I just read. It's going well in a lot of places around the world. But we've just started. This is we're nowhere near where we want to be. We want to get to 100 percent carbon neutral, which is that even possible? I think, of course, it is. But is it likely? Probably not. Not in anybody's reasonable lifetime. But but still, the work has to be done for the next generation.

S: All right. Now it's my turn to be a wet blanket. Ready?

J: Go ahead. Here you go. So we obviously cannot extrapolate into the future. That's what they did in 2005. And they were wrong. And I think that these trends are not going to be easy to sustain because I think that they represent picking a lot of technological, low hanging fruit. For example, a big part of this is replacing coal with natural gas, which was caused by fracking, making natural gas cheaper. That's pretty much it. Not really any plan or policy or anything. It's just well, except for allowing fracking. But there's nothing to replace natural gas with that is the equivalent of replacing coal with natural gas. And once you've done that, all we could do is just further get rid of coal. But then once we have a lot of natural gas, which releases methane and also releases some carbon, it's not going to be as easy to transition away from natural gas as it was to go from coal to natural gas. Also, the nuclear power, the big win in nuclear energy in the last 20 years was that they were able to extend existing nuclear power plants. But that's limited. They're only going to be able to do that for so much longer. In order to keep nuclear at 20 percent of our total generation, they're going to need to build nuclear power plants. And that's not happening. So we just delayed the inevitable with nuclear unless we significantly invest in next generation nuclear technology and renewables. Renewables are increasing wind and solar because they're super cheap, but they get more and more expensive as they get higher and higher percentage of our electricity production because you need more and more overcapacity or you need massive grid storage, which we don't have. So none of these trends that we've seen in the last 15 years are going to continue into the future. We need all new solutions going forward and we don't have them. And that's why I think we cannot just extrapolate. We're going to have to engineer to keep these trends going. We're going to have to build nuclear to get, in fact, expand our nuclear to get off of natural gas, because that's what natural gas can go to. We're going to need to update the grid, put in grid storage and build a lot of renewables. And we're going to need to keep pushing efficiency higher so that we keep demand under control. And then that's not I don't think any that's going to happen automatically. But as you say, it's hard to predict because other technologies might come into play that we're not factoring in now, and that will help. But we can't just count on that. You know what I mean? We need to engineer it.

E: What does it say that we've had many of the warmest years and on record over the course of this decrease in emissions?

S: It's not well, it's just we're still putting carbon into the atmosphere.

C: You know, we've also got more people.

S: We've just putting less. There's just less more carbon in the atmosphere than we thought we were going to have.

C: And remember, it accumulates of and it's not like it goes in and then it goes out. Every time we add carbon, it's accumulating because the oceans can't sink at all. The forest can't sink at all.

E: I suppose my point is that even despite these better habits that we seem to be getting into in some ways, it's still not having the impact on the environment that we need it to have.

S: Evan, to put it into perspective, if we had zero carbon emissions starting today, temperatures are still going to rise for decades from the carbon we've already put into the atmosphere.

E: Right.

S: Right?

C: And so we have to be coming up with efforts that actually actively reduce. When Jay said like, yeah, like Jay's like, I'm a bit cynical that we're going to get to carbon neutral. We need to actually be carbon negative.

S: Yeah.

J: Yeah, of course.

C: That's the only way this is actually going to level out.

S: But I'll take carbon neutral over putting more carbon.

C: Me too, me too.

E: Oh, well, sure. Yeah, you want to slow it. Yeah.

Sea Meadows Carbon Sink (1:05:39)[edit]

S: All right. And Cara, you have a quick sort of related news item about talking about carbon sinks, right? Because carbon carbon needs a place to go. And we think about trees and whatnot. But the ocean's a big carbon sink, too.

C: Yeah. So we know that the water itself is a carbon sink and we'll kind of get into that. But there's one aspect of the ocean that I don't think we often talk about, and that is seagrasses. Seagrasses are everywhere. They're on six of the or they're around six of the seven continents. And they make up these basically sea meadows or these sea forests. And the interesting thing is that seagrasses are enormous carbon sinks. They can store more than twice as much carbon per square mile as land forests do. And globally, their roots are thought to trap over 10% of the carbon that's buried in ocean sediment every year. Seagrasses also buffer against ocean acidification. We know that this destroys the calcium carbonate shells of a lot of species, including coral. And that's a huge and devastating result of carbon being sunk into the ocean, because obviously, once it is added to water H2O, it forms carbonic acid. So the oceans actually acidifies. The pH gets lower. And so they buffer against that. There is a study in 2021, just this year, that showed that along the California coast, seagrasses could potentially reduce local acidity by up to 30 percent across extended periods. And they also help with other things. They can help clean water. They can help support fisheries produce nurseries, protect coast from erosion, even trap microplastics. And they're literally everywhere. The problem is, when it comes to seagrasses, we have really limited data. There are huge holes in the data. Like when you look at maps, there are just whole areas that have never been mapped. So we really don't know how much seagrass we have on the planet. Really old estimates that are also incomplete say that maybe 300,000 square kilometers, so that translates to 115,000 square miles of seagrasses exist. Again, I mentioned six of the seven continents not including Antarctica. So it's about an area the size of Italy, if you were to add that together. But there could be much more that we haven't discovered. But here's the sad part. Human activity like pollution from mining, damage from fisheries, dredging, acidification, like I mentioned before, it destroys the equivalent of a soccer field of seagrasses every 30 minutes around the world.

E: Oh my gosh.

C: Yeah. According to the UN environmental program. And so here, here's an example. If we look at the last century, so the last hundred years in the UK, 92% of seagrasses disappeared and estimates show that if they were still here, 400 million fish could be supported and 11.5 million tons of carbon would have been captured. That's the same as 3% of their total emissions within the year. It's thought that seagrass meadows are being lost at a rate of 7% per year globally. And again, this is based on incomplete data. It could potentially be worse. So this is an example of a mitigation effort, a neutralization, maybe even a negativization. Yes, I made up that word effort that we have right in our backyard, but because of human activity, the same activity that's causing the climate crisis to begin with, we're also losing the very organisms that could help us buffer against our activity. And so A, we need to recognize this B we need to enact legislation and work very hard to protect the seagrasses that we have left. We spend a lot of time thinking and talking about the Amazon rainforest, which is fundamentally important to biodiversity. And it's fundamentally important to carbon sequestration. And of course, we're destroying it with gold mining, among other things, habitat loss, et cetera, et cetera. We can't also ignore these forests that exist within our oceans that are even potentially better at sequestering carbon. We can't let them fall by the wayside because they are not technologies we have to develop. They're already here. And so we need to protect them.

S: One more thing to worry about.

C: But also one more thing that if we do it the right way, it could be a boon.

S: That's true. Every problem is something that can be fixed that could make it better.

C: And the cool thing is if we, yeah, if we fix this problem, not only is the problem of the seagrasses going away fixed, but it also contributes to correcting some of the wrongs of climate change.

S: Yeah. All right.

Pharoah's Curse (1:10:14)[edit]

S: Evan, you brought this up to me, this next news item, and you said, you don't think we've ever talked about this on the show. And I, yeah, I don't remember that we have. Have we ever talked about the pharaoh's curse?

E: Good question. And I couldn't think of a time that we did, Bob, Jay?

J: Yeah, I'm already scared.

E: You should be scared. Well, when the documentary titled Abbott and Costello Meet the Mummy hit the silver screen in 1955, it brought up more questions than answers. Questions like what exactly is the pharaoh's curse and can the dead become animated? And did they really turn the tomb into a nightclub at the end of that movie? Well, we're going to put, so thank goodness we are now discussing this. We're going to put this long dry spell to rest and we can give thanks to recent news developments. Earlier this month in April, 22 mummies were transported from the Egyptian Museum in Tahir Square to their new home, the National Museum of Egyptian Civilization. And this was an elaborate royal procession. I don't know if you guys saw any video of them moving these mummies, but this thing was, well, they, they dubbed it the Golden Parade and it was elaborate to say the least. Spotlights everywhere, honor guards on horseback.There was a philharmonic orchestra to greet the royal remains as it arrived. The president of Egypt was performing the ceremonial duties and okay, it was, it's designed to spark and rekindle interest in Egypt's rich collections of antiquities. And certainly their tourism has almost entirely stalled because of what's happened with the coronavirus pandemic. So time to get people interested again and what better way than make a big celebration out of it. But moving the mummies is not without peril. Now I'm not talking about the physical remains or the sarcophagi in which they were contained, which is actually an interesting process. They, they put them into oxygen-free nitrogen-filled capsules on trucks with special shock absorbers to limit any damaging effects of actually transporting them and risking, and risk of humidity contamination or bacteria and insects and other things. So they really did a good job of keeping these things protected. But the ceremony has reignited talk of the Pharaoh's Curse. This curse is legendary. It is omnipresent and very much alive, even in the age of social media. For example, remember the ship that clogged up the Suez Canal for a week?

C: Oh, how could we not?

E: Just a couple of weeks ago, social media says, hey, this is part of the Pharaoh's Curse. And you can see all kinds of tweets and other things about people speculating that, yep, because they were getting ready to have this big ceremony and moving the mummies around, Pharaoh's Curse comes up again. Oh, also there was a tragic, a train crash occurred in the country and it killed a lot of people. This was just a few weeks ago. And what did they attribute that to? Yep, the Pharaoh's Curse. And a recent building collapse in central Cairo. There it is, the curse again, all in anticipation of these mummies being disturbed. So there was a lot of news surrounding it and about the Pharaoh's Curse as well. Now, NBC News, and I looked at a whole bunch of other news organizations, they all reached out to this gentleman. He seems to be the prominent Egyptian archaeologist, Zahi Hawass, former minister of state for antiquities affairs for Egypt. Dr. Hawass, who's an expert, has declared there's no Pharaoh's Curse. Okay. Well, that's a relief, but all right, what is the Pharaoh's Curse? And since we haven't talked about it, I'll go into it a little bit. Now, it's sometimes called King Tut's Curse, which maybe we've heard in, at some point, maybe in a Bugs Bunny cartoon a long time ago. King Tutankhamun's tomb was discovered in Egypt's Valley of the Kings back in late 1922. Wow, we're coming up on a hundred years. Time goes by quickly. But that incredible and historic discovery with it came a dreaded curse, which befell all those who dared disrupt the ancient kings buried over 3,000 years prior. So say it the legends and therefore it must be true, right? Now, is there any evidence though to back up the claims of a dreaded curse that lay upon all those involved in the discovery? Well, there is. First of all, they're all dead. So explain that. You can't. No, there are actually stories that helped develop the curse myth. This is back in 1923 in the following few years. So in the 1920s, this all sort of gelled together. We're familiar with the name Howard Carter? I would hope. He's the one most heavily credited with the discovery of King Tut's tomb.

C: Oh, wow. Cool.

E: Yep. Yep. So there's him, but he's not one of the, although eventually they attributed the curse to his death, which took place like 16 years later. But in any case, Carter had partners and a lot of people who obviously helped in the effort among them was, oh boy, George Edward, Stan Hope, Monteux Herbert, the fifth Earl of Carnarvon. Oh yeah, that's a mouthful. Now he, this guy was a British aristocrat as if I needed to explain that, but he had a more than passing interest in Egyptology. He was actually quite essential in making sure that this happened. Probably wouldn't have been possible without his backing. Now the Earl died on March 25th, 1923. This is very shortly after the discovery was made public. So how do we explain that? Must've been the curse, right? Well, he actually died from a mosquito carried disease, as did lots of people around the world at that time in history, but the Earl's half brother, Colonel Aubrey Herbert, who also entered the tomb at one point. Well, he died, died a few months after the Earl and towards, so how do you explain that one? Well, towards the end of Herbert's life, he became totally blind and he received some very bad medical advice, which persuaded him to have all of his teeth extracted to help restore his sight.

J: What?

E: Oh, so maybe he died as a result of infection from tooth removal?

J: I just, I find it hard that anyone would believe that.

C: That was a really common treatment for mental illness too. I mean, not common common, but yeah, it happened in asylums a lot.

E: It's horrific. Also led to a lot of health problems and death, obviously for people. There are, I won't bore you, but there are plenty of others. And in, within a few years, there were no fewer than nine people whom they associated either directly or through affiliations with the discovery of the tomb, who what they say is either died under mysterious circumstances or led to some sort of premature death. You have to understand, you can't underestimate what people will believe in any given age or time. I mean, a Pharaoh's curse, we think about it today. It has almost a cartoonish sort of feel to it. Who really even talks about the Pharaoh's curse anymore, but actually people do, they are out there and they are passing along that information and then at that level of belief. And it's not that strange because you still have people who believe in things like astrology and demonic possession and ghosts and lucky charms and superstitions and all sorts of things. So there's that on that background, maybe though, more importantly, number two, to give it in the proper context, the 1920s, this was a time where spirituality, seances and interest in the occult and paranormal were on the rise in a lot of Western societies and Britain in particular, which was just coming out of the horrors of World War I. The journalism at the time was sensational. Certainly there were false reports that started to emerge from the tomb. And of course that sold newspapers. So they ran with it. There was reasons to believe that there were booby traps on the tombs themselves, that they were poisoned and anyone who got near there was actually becoming poisoned or received some sort of microscopic infection. And this was all properly planned out by the Egyptians or the people who put them in the tombs from years ago, a trap waiting to go off. But obviously none of that bore any fruit or turned out to be truthful at all. Now, Carter himself, Howard Carter himself might bear some responsibility about the curse and its prevalence. Because he would remind people that curses were through both ceremonies and rituals and written warnings upon the tombs, the sarcophagi themselves, that these curses were in place. But there was a practical reason for that 3000 years ago, as it was in Carter's time when he made the discovery. And that was to what? Prevent looting, grave robbing. You had to concoct stories to get people to stop going in there to take these artefacts and things. So there's sort of this practical reason as to why you would want there to be a curse. But obviously people will take that to various degrees of seriousness. And then finally, when they've looked into it to declare that any significant number of people associated with discovery died prematurely or through mysterious means, it's nonsense. The numbers do not bear it out. It has been studied. In fact, one particular study in the 1930s, I believe, showed that they tracked 58 people who were present when the tomb and the sarcophagus were open. They tracked them over the course of their lives. And only eight had died within a dozen years. And statistically speaking, for the time that was right on par for the course, in fact, even a little bit better than average for what people were expected to live without the need for calling into effect a curse to make that explanation. So the curse of the pharaoh or the pharaoh's curse alive and well and still comes up any time you talk about mummies and these sorts of artefacts. And amazing to think that 100 years later, it's still prevalent.

S: Well, it's one of those just iconic things that's never going to go away.

E: Never.

S: The pharaoh's curse. And of course, there's a lot of cognitive bias behind it. The pattern recognition look, bad things happened. Like bad things don't happen. We don't need a pharaoh's curse to make bad things happen. That's just life.

C: Right. But we also we approach this from like a purely kind of secular scientific perspective. And of course, there are probably a fair amount of people who for whom spirituality and religion is like fundamental to their worldview. So it probably doesn't seem quite as bananas to them. It's so imbued in culture and society. They've been hearing it from the time they were born.

Who's That Noisy? (1:21:15)[edit]

  • Answer to last week’s Noisy: _brief_description_perhaps_with_link_

S: All right, Jay, it's Who's That Noisy time.

J: All right, guys, last week, I played this Noisy.

[_short_vague_description_of_Noisy]

Pretty cool, huh?

E: I love it.

J: You guys have had any idea?

E: Oh, gosh, I mean, it's a it's not. I don't think it's Orson Welles.

B: It's a dog making weird noises.

C: Wouldn't that be crazy? It's like a parrot. It's a parrot reading a news.

J: It's definitely it's from a time, a time that you get right. It's like from what what decades would you say this could possibly be?

S: Forties.

C: That's the radio?

J: Yes. Totally got that old school radio.

C: Yeah, yeah.

S: Totally.

J: All right. Well, we have some guesses. We haven't heard from Visto Tutti recently, and here's his guess. He says "This one is confusing. Had me analysing for ages. The recording may be old, but not as old as it seems. The musical theme is late 1960s, but the audio is artificially made to sound like the 40s. The actor affects a slight British tone in places, but inconsistently. So not natural. So I roll the dice. He's saying that it was Kolchak, the Night Stalker from 1974."

B: I love that show.

E: Wow.

J: Yeah, pretty, pretty cool guess. Not correct. But I do like the effort that you put into it. So you are still a warrior as far as I'm concerned. Michael Blaney wrote in and said, "Hi, Jay, it really sounds like the Twilight Zone, but with a skeptical twist, which is neat. The kind of show where there's some one on the wing." This is what he wrote. Something, remember? No? "If I had a hazard a guess, I'd say it's Rod Serling recording that never made it to the air, because sadly, no one wanted to see a skeptical version of the Twilight Zone." That is also incorrect, but a very fun guess. I have another guess. And this one happens to be the winner. Check this out. Michael Collier wrote in and said, "Hi, Jay, this week's noisy is a liar bird repeating an old recording from the Batman Mystery Club."

C: I just said, is it a bird?

J: It has nothing to do with the bird. He was just joking when he said that, because liar birds can mimic anything. So the answer is this is a recording from a radio show that never made it to the air called the Batman Mystery Club.

C: Cool.

J: So I will now defer to the person who sent this in. Octavio wrote in and said, "Back in the 1950s, there was an attempt to make a Batman radio show as a spinoff of The Adventures of Superman from the old radio show website article in 1950, an audition program was recorded, the Batman Mystery Club. Although Batman and Robin were featured in the program, it had little to do with the characters fans had come to know and was never broadcast." So that's really cool. Very interesting idea that they made a skeptical Batman and Robin Mystery Club radio show back then. You know, when I heard that voice, I'm like, oh, my God, this is really just it's so perfectly old school radio, and I just wanted everyone to hear it. So thank you, Octavio, for sending that in. Thanks, everyone, for your guesses.

New Noisy (1:24:26)[edit]

J: I do have a new Noisy. This Noisy was sent in by a listener named William Gru Mullins, and check this one out.

[_short_vague_description_of_Noisy]

It's got a long tail on there. So please be specific when you send in answers for this, because if you say that it's like a loud noise, that's not going to actually do anything for you. You can email me in at WTN@theskepticsguide.org. So I did see on Reddit that someone was asking like where they should submit emails to me, can you do an attachment? What's the ideal everything? So let me just give you the quick Who's That Noisy cheat sheet. One, email me at WTN@theskepticsguide.org. If you send it anywhere else, you have a very small chance that I'm going to actually use it, because I just go through my email at the appropriate time when I'm preparing the segment. Number two, you can absolutely send an attachment when you send an email to me to that email address. Number three, if you want to be nice, you could convert whatever it is into a WAV file for me, but you don't have to do it. I've never asked anyone to really even do that before. But if you want to, you can. That is the ideal state in which I prepare these. But someone on Reddit was asking. So there are all the answers. Please do send me in any cool noises you heard this week. And again, that's WTN@theskepticsguide.org.

NECSS (1:26:06)[edit]

S: All right, so, guys, we have NECSS coming up. And to help us talk about NECSS is the MC, George Hrab. George, how you doing, man?

G: Hi. Oh, I'm the MC. I'm the MC. That's right. Oh, my goodness. So exciting. How's everybody?

B: Good, man.

J: Hi George.

S: So we have a couple of things to talk about. I know we've been mentioning like a save the date for NECSS, but we have some actual updates. But George is going to start. We're actually going to solicit some things from our audience for the conference. George, tell them about it.

G: Yeah. So we were like thinking of doing something. We always do something on the night before NECSS. We always do the Friday night. There's like a preview thing. And even when and when we're in the virtual world, we still wanted to do a preview. Last year, we had a game show and some fun stuff. And this year, we're going to have a special keynote. But in addition to having a special keynote, we thought, wouldn't it be interesting? Wouldn't it be cool to get all of you out there involved and not you five on the SGU, but you out there listening, you with the headphones on right now? Maybe we can get you all involved. And we had this thought of over the last year. We've all been locked away. We've been in our homes. We've been we've been quarantined. And we're we're sure that some of you have come up with some interesting things over this time period, some interesting problem solvers, maybe an invention, maybe some kind of a art project, maybe some kind of a something that you finally had time to work on that thing you always wanted to work on. And you did it. Maybe you solved some problem that was happening in your garden. Maybe you designed some kind of rocket ship that could take you in safely to the grocery store to get jello, whatever you may have invented. We want to hear about it. And we're going to hear about it from you folks. And then we're going to feature the ones that we think are the most interesting and maybe the most sort of special. So basically Friday night, we're going to have a feature of cool stuff that you all out there in the wonderful SGU audience have invented. And the way you can get and be a part of this is sending us a video. Send us a two minute long video showing your invention, your fix, your your something that you cobbled together to make work better. Maybe that symphony that you wrote, maybe that that mural that you worked on in your kitchen or whatever it may be. Send us a two minute video. You can upload it to [NECSS.org/pandemicprojects]. And we're going to pick a bunch of you. And the coolest ones will feature on the Friday night pre-NECSS show. And we'll have you on live as well. And we'll chat with you. Won't that be fun? Guys, I am so excited for this.

S: Yeah, it could be a lot of fun. So what cool thing did you do during the pandemic that you otherwise would not have been able to do?

G: Yeah, yeah.

S: And it could be anything.

G: It could be anything.

J: George, I figured out how to gain a lot of weight.

C: Same.

G: The how to efficiently make cookies is pretty much what I was doing for last year.

E: And consume them.

G: And consume them. Right. Without even chewing. It's like a duck. I just sort of. Yeah. Entire tubes of cookies.

S: I've been doing a longitudinal study in binge watching. It's coming very well. I have all my data gathered.

G: OK, OK.

C: So wait, are these things supposed to be solutions to problems?

J: No, it could be anything.

S: It could be whimsical. They could be whimsical.

B: Think of it as your pandemic magnum opus. What's the coolest thing you created in the past?

G: That's really good.

J: And listen up. So we have speakers that I'm going to announce now. So we have Lena Tripathi, Dr. Robert Levy, George Church, Pete Echols. We're going to have someone from NASA come talk to us. And we have quite a few others coming. And on top of that, we have Paul Offit and Kevin Folta are going to be joining us. We're really excited. And on top of that, we are upgrading the technology. That's all I'm going to say. It's going to be cooler than last year.

G: How could it be cooler than last year? How is it even possible? How is it even possible!?

J: Ian and I didn't stop trying to improve it after after NECSS 2020. We kept talking about it and we kept coming up.

S: That was our pandemic challenge.

G: Yes, I hear you. Oh, cool. That'll be meta

S: We are looking for one particular speaker that we want our listeners help with. If anyone out there in SGU-

B: Can kidnap him?

S: -listening to this. No, but what we what we do need to either it could be you or you might know somebody who works for Boston Dynamics. We need an inside contact because we want somebody from Boston Dynamics to give us a presentation at NECSS. And it's kind of a hard nut to crack into without having knowing somebody or knowing somebody who knows somebody. So we're just we've decided to reach out to to our audience. This is really the last piece to the NECSS puzzle that we need to put into place. Everything else really is shaping up great.

J: And Steve, you know what? We never announced we actually have a title for NECSS 2021. It's called The Future Has Landed. That is our theme. The science and technology of today, that's amazing. That's what the whole conference is going to be about. We know you're going to love it. I'm super excited. I don't think I've ever been more excited for a NECSS conference than this one. So please join us. Go to NECSS.org and NECSS.org and register today.

S: Yeah. And the conference is August 6th and 7th. It's Friday and Saturday, August 6th and 7th. All right. Well, George, thanks for popping on the show to to help us talk about NECSS.

G: Oh, you know me. I'll always pop on to whatever I can.

S: Yeah, we do know that about you.

G: Thanks guys.

S: All right. Take care, George.

C: Thanks, George. See you.

Name that Logical Fallacy (1:31:49)[edit]

S: All right. We're going to do one Name That Logical Fallacy. This one comes from Alec, who writes, "I've listened to your podcast for a while now and love it. I got a question about a potential logical fallacy that I can't quite pinpoint. Living in Maryland, there are often discussions around the murder rate in Baltimore. Because of this, people will inevitably criticize any non-murder related legislative political actions for not addressing the murder problem. While this may be a valid way to criticize the city council's priorities, I don't believe it is a logical way to criticize the individual pieces of legislation as they were never designed to address the murder problem. Aside from this, the city council is certainly capable of addressing multiple issues at once. A current example of this is a proposal to add speed cameras along a major highway that enters the city. Personally, I've seen a few people criticize the proposal itself and said most people criticize it for not addressing the murder problem. This feels like a logical fallacy to me, but I'm not sure. Specifically, it makes me think of a false dichotomy. But again, I'm not confident in this assessment. Could you provide some insight?" So what do you guys think about this kind of fallacy?

C: It's a straw man. No?

S: No.

E: You can chew gum and walk at the same time.

C: Oh, see, I was reading it as it's not fair to criticize a piece of legislation that was never designed to solve that problem anyway. That would be a straw man argument.

S: Yeah, but they're saying that's part of it. Again, these are informal logical fallacies. They all blend into each other. But he's focusing on the fact that it's not just that you're criticizing it for not doing something it wasn't designed in the first place. You're criticizing it because it's not addressing this more important problem. So nothing is valuable unless it's fixing the murder problem in Baltimore. But of course, this could apply to a lot of things. It's like, why are we sending people to the moon when there are hungry people?

C: Is that moving the goalpost? No. Which one is that?

E: No, no.

C: Which one is that?

S: No.

C: I'm just blanking. I know exactly what this is.

S: I wrote an article about this fallacy because it often gets applied to skeptics like why are you debunking Bigfoot? Aren't there more important things to do out there? So this is called the fallacy of relative privation. That's the name of the fallacy, relative privation. And because there's always something more important that you could point to out there. And again, where it gets tricky is when you're applying it to an individual person or group or specific bill or whatever. It's one thing to say that as a society, we need to have our priorities and we need to decide where we're going to put our resources. But if you're saying like, why are you doing this? Aren't there more important things to do? It's you know, it is a fallacy. It's ridiculous. So everybody should be trying to cure childhood cancer. Nobody should be doing anything until we decide what the one most important problem is in the world. And we all should focus on fixing that before we move on to the next thing. There's a lot of reasons why you might choose to do other things like opportunities, talent, skill-

B: Desire.

S: -desire. Yeah, it's all fine. And because something is not as important as something else doesn't mean it's not important. As Evan was getting close to it with the the false choice thing, there's a yes, we can walk and chew gum at the same time. We can fix more than one thing or address more than one issue at the same time. But it's often just a lazy way of criticizing something that you may not like for other reasons to say, well, there are more important things that you should be spending your time on. Or that we should be spending our resources on or whatever. And it's like, yeah, we could do multiple things. And they just if it's valuable, it's valuable. If it's a good idea, it's a good idea. It doesn't matter that there are that there are relatively more important things out there. And then importance can often be subjective, not absolute. And again, there are other criteria that might determine where it's best to put your efforts. So relative privation. Another manifestation of this might be, Cara, I think you'll appreciate this, is that like, oh, why are you worried about this form of racism or sexism? We're not hanging people anymore. Yeah, it's like there are the like systematic discrimination is gone now. So you're complaining about smaller and smaller problems. It's like, yeah, but that doesn't mean these aren't real problems. Just because they were just because there were worse problems in the past.

C: Well, or I should even say just sometimes more obvious problems.

S: Yeah, whatever. But even if there were like, yes, yes, yes. Slavery was worse than whatever we have today. Yes, absolutely. But just because we're not fighting slavery anymore doesn't mean that there's nothing worth fighting today, right?

C: Yeah.

S: And it's the same with, I think, a lot of social progress is that, yeah, it will we will focus on relatively smaller and smaller problems. That's a marker of progress. It doesn't mean they're not worth addressing just because they were even worse problems in the past. That's a relative privation fallacy as well. All right. Let's move on with science or fiction.

Science or Fiction (1:36:54)[edit]

Item #1: A review of data from 2020 finds that death by suicide fell by 6% in the US, with similar numbers in other developed nations.[6]
Item #2: The Princeton Plasma Physics Lab has developed a room temperature plasma for consumers that can kill 99.99% of bacteria on surfaces.[7]
Item #3: A recent fMRI study of the brains of violent criminal psychopaths and healthy controls could find no significant difference in brain function.[8]

Answer Item
Fiction Brains of violent criminals
Science Death by suicide fall
Science
Room temperature plasma
Host Result
'
Rogue Guess
Evan
Brains of violent criminals
Cara
Brains of violent criminals
Bob
Brains of violent criminals
Jay
Brains of violent criminals

Voiceover: It's time for Science or Fiction.

S: Each week, I come up with three science news items or facts, two real and one fake. And then I challenge my panel of skeptics to tell me which one is fake. Just three news items this week. No theme. Is everyone ready?

J: Let's do it.

S: All right. Here we go. Item number one, a review of data from 2020 finds that death by suicide fell by six percent in the U.S. with similar numbers in other developed nations. Item number two, the Princeton Plasma Physics Lab has developed a room temperature plasma for consumers that kill ninety nine point nine nine percent of bacteria on surfaces. And on number three, a recent FMRI study of the brains of violent criminal psychopaths and healthy controls could find no significant difference in brain function. Evan, go first.

Evan's Response[edit]

E: 2020 death by suicide fell six percent in the U.S. OK. I mean, we're talking about the year of coronavirus, obviously, and a lot of mental health issues that came hand in hand with that. So this would run perhaps counterintuitive to that. But that doesn't necessarily mean that that that is what actually happened. Suicide may have fallen because other parts of society, as the coronavirus shut it down, meant that people weren't, say, being bullied as much because of the lack of social interaction and other things that lead to suicide. So perhaps that one's right. Then this the next one, Princeton Plasma Physics Lab, a room temperature plasma killing ninety nine point nine nine percent of bacteria on surfaces. Room temperature plasma. I bet you Bob will have some interesting things to perhaps say about that. And then the last one, the FMRI study of the brains of violent criminal psychopaths. Ouch. And healthy controls could find no significant difference in brain function, no significant differences, I suppose, in any aspect of brain functions is how I'm interpreting this. I'll go with the fMRI study. They must have been able to detect some perhaps some significant difference in brain function. It just seems too broad how it's worded here. So I have a feeling that somewhere in there, there's the truth. So that one's fiction.

S: OK, Cara.

Cara's Response[edit]

C: I absolutely agree with Evan. I've seen too many studies that show the difference. So, yeah, maybe one study showed it. I mean, that's the hardest thing when you word them this way. A recent fMRI study of what? Like three people? Sure. Any study is going to show no no difference or a significant difference. It's when you actually look at all of the literature together. So it kind of is like, I don't know, that's a red flag to me. But absolutely, psychopathy is characteristic. Absolutely. I think plasma plasma is like a gas, right? Or not quite a gas, but like a liquidy gas, which I did think was supposed to be hot. But maybe there's like a super concentrated gas or something as a plasma. Yeah, why not? I mean, we can kill stuff with light or with certain UV measurements. And yeah, I have a feeling that we're going to see, sadly, a really big spike in suicides in 2021 as as things start to go back to "normal". I actually wouldn't be surprised if there were fewer suicides during lockdown, but that the rate would actually go up and maybe even go up past what we're used to seeing this year and next year, which bums me out. But I think that that's that's what the data probably will bear out. So, yeah, I'm going to go with Evan. I just there's just so much evidence to show that their brains are different.

S: OK. And Bob.

Bob's Response[edit]

B: Death by suicide fell by six. I thought I thought I read somewhere that it went up in 2020 and it just didn't make any sense. Or maybe it was maybe that was just murders. I don't know. Something went up. Let's look at the plasma plasma is basically atoms that have been ripped apart, like charged particles free, electrons and and other particles and and protons. So, yeah, that's like the most common matter in all of the universe. Stars are made out of plasma. But yeah, cool plasma. I think, yeah, I think that trying to. So, yes, it seems counterintuitive. How could something that could rip apart atoms be kind of room temperature? But I think that can be done trying to think of specifically how they would do that. But so I think that that is possible. It's meant to throw us off. So, yeah no fMRI. I mean, that could at first blush. It seems kind of like like a coarse kind of way to observe the brain doesn't necessarily can show psychopathic brains. But I think Cara and Evan kind of swayed me in this direction. I'll do a GW EC. So I'll say fMRI is fiction as well.

S: And Jay.

Jay's Response[edit]

J: Yeah. So quickly going through these the death by suicide fell by six percent. I'm curious to know if that's true. Like, what would be the reason? You know, I'm just thinking very even though the pandemic has been really stressful, people have been a lot less stressed out about their work situation. So, yeah, I don't know. That's interesting. I mean, I would tend to think that the less time people are actually physically at work, the happier they are. So that's probably true. The plasma one sounds really cool. I'd like to know exactly how it's used. Like, what do they do with it? You know, if it's for consumers, like, what do you just leave it? I don't know. What do you do with it? Do you rub it on your hands, rub it around? What do you do?

S: Spray it on stuff.

J: You spray plasma on stuff. OK, but just don't drink it. That's interesting. I'd like to know what it is that makes it antibacterial. And then this last one. I mean, I would tend to think that there would be a very significant difference between violent criminals and people who aren't violent criminals, at least something that would be detectable.

B: Not just violent, psychopathic.

J: Yeah, psychopathic violent criminals like that. An fMRI, you'd think if there's ever an instrument that we would be able to measure that it would be that one. So out of the three, that's the one that definitely stands out to me. So I will say that one is the fiction.

Steve Explains Item #2[edit]

S: All right. So you guys are all in agreement. So let's start with number two here. The Princeton Plasma Physics Lab has developed a room temperature plasma for consumers that killed 99.99% of bacteria on surfaces. You all think this one is science and this one is science.

J: Cool.

C: That sounds awesome. Is it expensive?

S: Didn't say anything about price. This is just sort of a proof of concept kind of study. They also say if you combine it with hydrogen peroxide, it kills 99.9999% of bacteria.

C: Yeah, but you could also just wipe things down.

S: Yeah. Well, it's not going to kill. If you just wipe things down with like water, you're just going to move it around. You're not going to kill all the bacteria.

C: No but like bleach. We have bleach.

E: Lysol.

S: Lyson will do it. Yeah, Lysol will do it.

C: But yeah, it's like you can already just spray a can of Lysol on stuff.

B: Yeah, but plasma.

E: This is plasma. Lysol plasma.

J: Why do the plasma route, Steve? Did they say like why they invented it?

S: Well, I think they're just trying to come up with another consumer product. That will do the same thing. This is a, it's room temperature and normal atmospheric pressure. They still are good. They haven't tested it for viruses yet, but they suspect it will also be affected for viruses. Obviously, that would be a nice thing to have during a pandemic, a viral pandemic.

Steve Explains Item #3[edit]

S: But all right, let's go to number three. A recent fMRI study of the brains of violent criminal psychopaths and healthy controls could find no significant difference in brain function. You guys all think this one is the fiction. So clearly there are differences. I mean, there's no one could reasonably argue that there isn't a difference. It's a personality disorder. The question is, is it a difference that could be imaged on fMRI scan?

C: Well, it has before.

S: And specifically with the paradigm that they used in this study [inaudible].

C: Right. I mean-

S: -looking for that's the question.

C: And that's a shot in the dark. Maybe, maybe not.

S: So this one is the fiction.

E: OK.

J: Nice.

C: Yes, yes, yes, yes.

S: Yeah. For the reasons that you said. So what the study found was really big differences. So they looked at anatomically and with fMRI scan. They did regular MRI and they did fMRI. And they found that they watched. Yeah. They watched videos of violent bad things happening. Their emotional centers did not get activated in the same way that healthy controls did.

B: That makes sense.

S: On fMRI. Yeah, it makes perfect sense. This study also found differences in well functioning individuals who have personality traits associated with psychopathy. So even if you're not a violent criminal, but you had you like score high on the psychopath test, you still will have differences in your brain. And so to clarify what they found. So it was the control of the emotional areas that was compromised. So their emotional reaction was actually higher because they lacked the the brain regions that would moderate and control the emotional.

C: So they couldn't inhibit a reaction to violence.

S: They can't. Yeah, they couldn't inhibit it. That's why they tend to be impulsive and callous. They don't have the the inhibitory control.

C: Right. Like, why did you shoot that person? They were in my way. That kind of.

S: Yeah. Yeah.

E: Why did some brains develop that way?

C: I mean, that is a really interesting question. Yeah.

S: Everything that can go wrong in the body goes wrong.

C: Yeah. Just read some Oliver Sacks. By the way, have you guys seen the documentary on PBS?

S: I haven't seen it yet.

B: About Sacks?

C: Yeah, about Sacks.

B: I bet that's good.

C: It's great.

E: That I would want to see.

C: Yeah. Check it out. It's out now.

Steve Explains Item #1[edit]

S: All this means that a review of data from 2020 finds that death by suicide fell by six percent in the U.S. with similar numbers in other developed nations is science. And yeah, there was a lot of speculation about what was what the suicide rate was going to do during the pandemic because there's a lot of a lot of psychological stress associated with it. But in fact, it went down and I stress this was in, like developed nations with the exception of Japan where there was, I think, a slight increase.

C: But there's also a lot of weird exceptions with Japan and suicide. Cultural exceptions.

S: Yeah, exactly. They're they're an outlier baseline. And the U.S. had the biggest drop of six percent. But again, other similar nations. The idea is that it was probably when any kind of catastrophe or or a bad situation hits, there's an initial heroic stage where everyone sort of banding together.

C: And that's why I think this year next year is probably not going to look good.

S: Yeah. So there's definitely worry about a rebound. But also people may have been spending more time with family members and being under more careful observation just because they're not going out.

C: Yeah. And there's a protective mechanism. I mean, there's a protective factor of being around friends and family. The problem is that the people who are really isolated and who maybe are experiencing anhedonia and who are experiencing like low energy, that kind of pandemic fatigue that a lot of us are dealing with. I mean, you see similar things in the course of a bipolar disorder. If somebody sadly does die by suicide, it's often not as they're going down, it's as they're coming back out of it. And so, yeah, that's something similar here.

S: But they also here's one thing that may be sustainable is that they say it may also be the dramatic increase in the availability of telehealth services.

C: Yey! Hurray!

S: So if that's the case, if that turns out to be the case, that's something that should persist.

C: Yeah. Yeah.

E: Expand it.

S: Yeah, totally.

C: That's wonderful.

S: No, it's the best single thing to come out of the pandemic was the explosion of telehealth services in my completely biased opinion.

C: Mine, too. Mine, too.

S: But, yeah, it's been great. And so that would be if they can focus, if they could identify that as a significant factor here, that would be a further boost.

C: So many more people. Yeah. So many more people are able to be reached if they don't have to drive across town or get a babysitter all those different reasons.

S: It's also what my wife did, her Ph.D. in tele-mental health. And basically her research found that it's just as effective as in person.

B: You're so biased.

E: Great. That's great.

Skeptical Quote of the Week (1:49:37)[edit]


Common sense is a very tricky instrument. It is as deceptive as it is indispensable.

 – Susanne Katherina Langer (1895-1985), American philosopher, writer, and educator


S: All right, Evan, give us a quote.

E: All right. Before I say the quote, I want to have each of you kind of give me your quick opinion on what you think about this quote, because I've had some thoughts about this very point over my years. "Common sense is a very tricky instrument. It is as deceptive as it is indispensable." And that was written by Suzanne Katharina Langer. She was an American philosopher. She was born in 1895. She died in 1985. She was a writer and educator well known for her theories on the influences of art on the mind. She was one of the first women in American history to achieve an academic career in philosophy and the first woman to be popularly and professionally recognized as an American philosopher. She was elected as a fellow to the AAAS in 1960. So perhaps a forgotten superhero of science there. But at the same time, the quote itself, this is something I've thought about as well. And common sense for me is kind of an OK, a fair starting point, but you can't rely on it to make any final conclusions on things. How do you feel about that?

S: No, I agree that I think it's a very, a very wise quote. Because common sense, it's like what Cara, like what we would call face validity, right? Like it's it's a starting point.

C: It's like you need that first.

S: Yeah. Like if somebody doesn't have like make even basic sense at a fundamental level, you should be very skeptical of it. But it could be very deceptive because "common sense" could just be a manifestation of your cognitive biases. It could all be confirmation bias.

C: It's like are we talking about common sense or critical common sense?

S: It's kind of like intuition. Intuition can get you 90 percent of the way there a lot of the time. But you have to back it up with with analysis, with critical analysis, because it's often quite deceptive as well.

B: Also, it reminds me of humor. No one wants to think they don't have a sense of humor. And similarly, I don't think anyone wants to think or will believe that they don't have common sense.

J: Yeah. I mean, I think it would take an enormous amount to convince someone that they don't have common sense. They'd have to have like they would have to have proven to themselves over and over again. But typically people can't see that or admit that.

S: But if you have a complete absence of common sense, it makes you vulnerable to things like believing the world is flat. Things that you should be rejecting on their face. You will. You could say, hey, maybe this is true. No, it's true.

C: Yeah. Like so many types of like pseudoscientific treatments or devices where so often we're like, well, how would that even work? Like, it's so easy to just be like, that doesn't sound right. But many people like that doesn't make scientific sense, but many people who don't have that basic filter wouldn't know that.

S: Yeah. All right, guys. So we will be doing a Friday live stream going forward. We're still continuing to do that. Thank you guys for joining me this week.

B: Sure, man.

J: You got it, brother.

C: Thanks Steve.

E: Thank you, Steve.

Signoff/Announcements[edit]

All right, guys, so we will be doing a Friday live stream that going forward to do that. Thank you guys, for joining me this week. Your man, you got a brother named Steve

S: —and until next week, this is your Skeptics' Guide to the Universe.

S: Skeptics' Guide to the Universe is produced by SGU Productions, dedicated to promoting science and critical thinking. For more information, visit us at theskepticsguide.org. Send your questions to info@theskepticsguide.org. And, if you would like to support the show and all the work that we do, go to patreon.com/SkepticsGuide and consider becoming a patron and becoming part of the SGU community. Our listeners and supporters are what make SGU possible.

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